OBJECTIVE: To investigate whether myocardial beta-adrenoceptor (beta-AR) downregulation precedes and predicts left ventricular (LV) dilation after acute myocardial infarction (AMI), we measured beta-AR density within four weeks of AMI and correlated it with serial measurements of LV volumes. BACKGROUND: Patients who develop heart failure following AMI have an increased sympathetic drive to the heart within the first four weeks after infarction. METHODS: We prospectively studied 61 patients in whom AMI was the first presentation of coronary artery disease (CAD) and with no signs of heart failure. The LV volumes were measured one, three, and six months after AMI by echocardiography. Beta-AR density was measured using positron emission tomography with S-[(11)C]CGP 12177. Seventeen matched healthy volunteers served as controls. RESULTS: Whole heart beta-AR density was lower in patients than in controls (6.25 +/- 0.98 pmol/g vs. 8.32 +/- 2.14 pmol/g, p < 0.0001). In patients, beta-AR density was inversely correlated with end-systolic and end-diastolic volumes six months after AMI. Patients whose LV was dilated at six months had a lower beta-AR density in noninfarcted myocardium than patients without dilation (6.15 pmol/g vs. 6.98 pmol/g, p = 0.008). In addition, beta-AR density in noninfarcted myocardium was higher when the infarct-related artery was patent (6.87 +/- 1.14 pmol/g vs. 5.76 +/- 0.86 pmol/g occluded, p < 0.01). CONCLUSIONS: Myocardial beta-AR density is reduced after AMI in the absence of heart failure, and the reduction predicts later LV dilation. These data are suggestive of an enhanced sympathetic drive to the heart, having an important etiologic role in LV remodeling after AMI.
OBJECTIVE: To investigate whether myocardial beta-adrenoceptor (beta-AR) downregulation precedes and predicts left ventricular (LV) dilation after acute myocardial infarction (AMI), we measured beta-AR density within four weeks of AMI and correlated it with serial measurements of LV volumes. BACKGROUND:Patients who develop heart failure following AMI have an increased sympathetic drive to the heart within the first four weeks after infarction. METHODS: We prospectively studied 61 patients in whom AMI was the first presentation of coronary artery disease (CAD) and with no signs of heart failure. The LV volumes were measured one, three, and six months after AMI by echocardiography. Beta-AR density was measured using positron emission tomography with S-[(11)C]CGP 12177. Seventeen matched healthy volunteers served as controls. RESULTS: Whole heart beta-AR density was lower in patients than in controls (6.25 +/- 0.98 pmol/g vs. 8.32 +/- 2.14 pmol/g, p < 0.0001). In patients, beta-AR density was inversely correlated with end-systolic and end-diastolic volumes six months after AMI. Patients whose LV was dilated at six months had a lower beta-AR density in noninfarcted myocardium than patients without dilation (6.15 pmol/g vs. 6.98 pmol/g, p = 0.008). In addition, beta-AR density in noninfarcted myocardium was higher when the infarct-related artery was patent (6.87 +/- 1.14 pmol/g vs. 5.76 +/- 0.86 pmol/g occluded, p < 0.01). CONCLUSIONS: Myocardial beta-AR density is reduced after AMI in the absence of heart failure, and the reduction predicts later LV dilation. These data are suggestive of an enhanced sympathetic drive to the heart, having an important etiologic role in LV remodeling after AMI.
Authors: Grace P Chen; Ramin Tabibiazar; Kelley R Branch; Jeanne M Link; James H Caldwell Journal: J Nucl Cardiol Date: 2005 Nov-Dec Impact factor: 5.952